Obesity is an independent risk factor of cardiovascular diseases. Epidemiological studies have shown that obesity induces the production of inflammatory factors and changes in cardiac hemodynamics, remodeling and function, leading to myocardial damage and heart diseases. The positive effect of exercise on the cardiovascular system has been widely confirmed, while the acute cardiovascular stress caused by exercise cannot be ignored. Compared with the general population, obese people were more prone to arrhythmia and have a higher risk of cardiovascular events during exercise, due to their abnormal cardiac function, myocardial pathological remodeling and low tolerance to corresponding stress. Studies have shown that the intervention of exercise preconditioning (EP) can effectively reduce such risks. EP increases myocardial oxygen consumption through short-term exercise, resulting in relative or absolute myocardial ischemia, inducing the intrinsic myocardial protective effect and reducing the continuous ischemia caused by subsequent long-term exercise. This article reviews the obesity-induced abnormal changes of cardiac function and structure, possible exercise- induced risks of cardiovascular events in obese people and the role of EP in reducing exercise-induced risks of cardiovascular events. We summarize the progress on EP models in obese people, EP prevention against adverse cardiovascular events in obese people, with the aim to provide a theoretical basis for the application of EP in obese people.
Humans ; Exercise ; Obesity ; Myocardium/pathology* ; Myocardial Ischemia ; Cardiovascular Diseases

Fatty Liver ; etiology ; pathology ; Humans ; Liver Cirrhosis ; etiology ; pathology ; Obesity ; complications ; pathology ; therapy ; Risk Factors

Obesity is characterized by abnormal and excessive adipose tissue accumulated in the body. Compared with peripheral obesity (the accumulation of subcutaneous adipose tissue), abdominal obesity (the accumulation of visceral adipose tissue) is associated with increased risk of the metabolic syndrome, such as diabetes, hypertension, atherosclerosis, and dyslipidemia. Adipose tissue is a highly heterogeneous endocrine organ. Adipose tissue depots differ significantly in anatomy, cell biology, glucose and lipid metabolism as well as in endocrine regulation. Visceral adipose tissue has a stronger metabolic activity and secrets a larger amount of free fat acids, adipocytokines, hormones and inflammatory factors, which flux into the liver directly via the hepatic portal vein. These characteristics indicate that visceral adiposity may lead to the metabolic syndrome and thus visceral adipose tissue might be the clinical target for the prevention and treatment of obesity.
Adipose Tissue ; pathology ; Humans ; Intra-Abdominal Fat ; pathology ; Lipid Metabolism ; Metabolic Syndrome ; physiopathology ; Obesity ; physiopathology ; Obesity, Abdominal ; physiopathology ; Subcutaneous Fat ; pathology

Obesity is an important risk factor for cardiovascular diseases, which can lead to a variety of cardiovascular diseases including myocardial remodeling. Obesity may induce myocardial dysfunction by affecting hemodynamics, inducing autonomic imbalance, adipose tissue dysfunction, and mitochondrial dyshomeostasis. The key necessary biochemical functions for metabolic homeostasis are performed in mitochondria, and mitochondrial homeostasis is considered as one of the key determinants for cell viability. Mitochondrial homeostasis is regulated by dynamic regulation of mitochondrial fission and fusion, as well as mitochondrial cristae remodeling, biogenesis, autophagy, and oxidative stress. The mitochondrial fission-fusion and morphological changes of mitochondrial cristae maintain the integrity of the mitochondrial structure. The mitochondria maintain a "healthy" state by balancing biogenesis and autophagy, while reactive oxygen species can act as signaling molecules to regulate intracellular signaling. The excessive accumulation of lipids and lipid metabolism disorder in obesity leads to mitochondrial dyshomeostasis, which activate the apoptotic cascade and lead to myocardial remodeling. In this review, we provide an overview of the recent research progress on obesity-induced myocardial remodeling and its possible mechanism of mitochondrial dyshomeostasis.
Humans ; Mitochondria ; pathology ; Mitochondrial Dynamics ; Myocardium ; pathology ; Obesity ; physiopathology ; Reactive Oxygen Species

Objective: To investigate the effect of visceral fat area (VFA) on the surgical efficacy and early postoperative complications of radical gastrectomy for gastric cancer. Methods: A retrospective cohort study method was used. Clinicopathological data and preoperative imaging data of 195 patients who underwent D2 radical gastric cancer surgery at the First Affiliated Hospital of Xi'an Jiaotong University from January 2014 to December 2017 were analyzed retrospectively. Inclusion criteria: (1) complete clinicopathological and imaging data; (2) malignant gastric tumor diagnosed by preoperative pathology, and gastric cancer confirmed by postoperative pathology; (3) no preoperative complications such as bleeding, obstruction or perforation, and no distant metastasis. Those who had a history of abdominal surgery, concurrent malignant tumors, poor basic conditions, emergency surgery, palliative resection, and preoperative neoadjuvant therapy were excluded. The VFA was calculated by software and VFA ≥ 100 cm² was defined as visceral obesity according to the Japan Obesity Association criteria . The patients were divided into high VFA (VFA-H, VFA≥100 cm², n=96) group and low VFA (VFA-L, VFA<100 cm², n=99) group . The clinicopathological characteristics, surgical outcomes and early postoperative complications were compared between the two groups. Univariate and multivariate Logistic regression models were used to analyze the risk factors of early complications. Receiver operating characteristic (ROC) curve was used to analyze predictive values of VFA for early complications. Pearson's χ² test was used to analyze the correlation between BMI and VFA. Results: There were no significant differences in terms of gender, age, American Society of Anesthesiologists physical status classification, preoperative comorbidities, preoperative anemia, tumor TNM staging, N staging, T staging and tumor differentiation, surgical method, extent of resection, and tumor location between the VFA-L group and the VFA-H group (all P>0.05). However, patients in the VFA-H group had higher BMI, larger tumor, lower rate of hypoalbuminemia and greater subcutaneous fat area (SFA) (all P<0.05). The VFA-H group presented significantly longer operation time and significantly less number of harvested lymph nodes as compared to the VFA-L group (both P<0.05). However, there were no significant differences in intraoperative blood loss, conversion to laparotomy and postoperative hospital stay (all P>0.05). Complications of Clavien-Dindo grade II and above within 30 days after operation were mainly anastomosis-related complications (leakage, bleeding, infection and stricture), intestinal obstruction and incision infection. The VFA-H group had a higher morbidity of early complications compared to the VFA-L group [24.0% (23/96) vs 10.1% (10/99), χ²=6.657, P=0.010], and the rates of anastomotic complications and incision infection were also higher in the VFA group [10.4% (10/96) vs. 3.0% (3/99), χ²=4.274, P=0.039; 7.3% (7/96) vs. 1.0% (1/99), P=0.033]. Multivariate logistic analysis showed that high BMI (OR=3.688, 95%CI: 1.685-8.072, P=0.001) and high VFA (OR=2.526, 95%CI: 1.148-5.559,P=0.021) were independent risk factors for early complications. The area under the ROC curve (AUC) of VFA for predicting early complications was 0.645, which was higher than that of body weight (0.591), BMI (0.624) and SFA (0.626). Correlation analysis indicated that there was a significantly positive correlation between BMI and VFA (r=0.640, P<0.001). Conclusion: VFA ≥ 100 cm² is an independent risk factor for early complications after radical gastrectomy for gastric cancer.It can better predict the occurrence of above early postoperative complications.
Gastrectomy/methods* ; Humans ; Laparoscopy/methods* ; Lipids ; Obesity/surgery* ; Obesity, Abdominal/surgery* ; Postoperative Complications/epidemiology* ; Retrospective Studies ; Stomach Neoplasms/pathology*

This study tested the effects of the gastrointestinal pulse train electrical stimulation with different parameters and at different locations on the neuronal activities of the lateral hypothalamus area (LHA) in obese rats in order to find the optimal stimulation parameter and location. Eight gastric electrical stimulations (GES) with different parameters were performed and the neuronal activities of gastric-distension responsive (GD-R) neurons in LHA were observed. The effects of stimulations with 8 parameters were compared to find the optimal parameter. Then the optimal parameter was used to perform electrical stimulation at duodenum and ileum, and the effects of the duodenal and ileac stimulation on the GD-R neurons in LHA were compared with the gastric stimulation of optimal parameter. The results showed that GES with the lowest energy parameter (0.3 ms, 3 mA, 20 Hz, 2 s on, 3 s off) activated the least neurons. The effects of GES with other parameters whose pulse width was 0.3 ms were not significantly different from those of the lowest energy parameter. Most gastric stimulations whose pulse width was 3 ms activated more LHA neurons than the smallest energy parameter stimulation, and the effects of those 3 ms gastric stimulations were similar. Accordingly, the lowest energy parameter was recognized as the optimal parameter. The effects of stimulations with the optimal parameter at stomach, duodenum and ileum on the LHA neuronal activities were not different. Collectively, gastrointestinal electrical stimulation (GIES) with relatively large pulse width might have stronger effects to the neuronal activities of GD-R neurons in LHA of obese rats. The effects of the GIES at different locations (stomach, duodenum and ileum) on those neurons are similar, and GES is preferential because of its easy clinical performance and safety.
Animals ; Duodenum ; pathology ; physiopathology ; Electric Stimulation ; Hypothalamus ; pathology ; physiopathology ; Ileum ; pathology ; physiopathology ; Male ; Neurons ; metabolism ; pathology ; Obesity ; chemically induced ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Stomach ; pathology ; physiopathology

Adult ; Female ; Humans ; Liver ; pathology ; Male ; Middle Aged ; Non-alcoholic Fatty Liver Disease ; pathology ; Obesity ; pathology ; Young Adult

OBJECTIVETo investigate the impact of obesity and hypertension on the size of the left atrium.

METHODSA total of 383 subjects were divided into normal group (NS, n = 95), hypertension group (HT, n = 97), obesity group (OB, n = 98) and hypertension with obesity group (HT + OB, n = 93). Clinical information, echocardiographic parameters and left atrial size in the four groups were compared.

RESULTS(1) The left atrial volume index (LAVI) was arranged in the order: HT + OB > OB > HT > NS (28.07 ± 6.63 > 24.61 ± 4.89 > 22.73 ± 5.16 > 19.18 ± 4.82 ml/m, P < 0.05); Difference on LAVI was significant in four groups after adjusting for age, gender, HR, FPG, TC, TG and HDL (P < 0.05). (2) Pearson correlation analysis showed closer correlation between BMI with LAVI compared to SBP and DBP with LAVI (r values: 0.505, 0.240, 0.209, P < 0.001). After adjusting for other factors, the correlation between BMI and LAVI remains significant (β = 0.411, P < 0.001) while no significant relationship between SBP, DBP and LAVI was found. One unit BMI increase is associated with 0.052 cm enlargement of left atrial diameter (LAD), 1.053 ml increase of left atrial volume (LAV) and 0.710 ml/m increase of LAVI.

CONCLUSIONThe impact of obesity on the size of left atrium is greater than that of hypertension. Obesity and hypertension have synergistic effects on enlarging left atria.

Adult ; Anthropometry ; Female ; Heart Atria ; pathology ; Humans ; Hypertension ; complications ; pathology ; Hypertrophy ; Male ; Middle Aged ; Obesity ; complications ; pathology

PURPOSE: The purpose of this study was to develop a system dynamics model for adolescent obesity in Korea that could be used for obesity policy analysis. METHODS: On the basis of the casual loop diagram, a model was developed by converting to stock and flow diagram. The Vensim DSS 5.0 program was used in the model development. We simulated method of moments to the calibration of this model with data from The Korea Youth Risk Behavior Web-based Survey 2005 to 2013. We ran the scenario simulation. RESULTS: This model can be used to understand the current adolescent obesity rate, predict the future obesity rate, and be utilized as a tool for controlling the risk factors. The results of the model simulation match well with the data. It was identified that a proper model, able to predict obesity probability, was established. CONCLUSION: These results of stock and flow diagram modeling in adolescent obesity can be helpful in development of obesity by policy planners and other stakeholders to better anticipate the multiple effects of interventions in both the short and the long term. In the future we suggest the development of an expanded model based on this adolescent obesity model.
Adolescent ; Humans ; Internet ; *Nonlinear Dynamics ; Obesity/*pathology ; Republic of Korea ; Risk Factors ; *Risk-Taking ; Surveys and Questionnaires

5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that was originally identified as the key player in maintaining cellular energy homeostasis. Intensive research over the last decade has identified diverse molecular mechanisms and physiological conditions that regulate the AMPK activity. AMPK regulates diverse metabolic and physiological processes and is dysregulated in major chronic diseases, such as obesity, inflammation, diabetes and cancer. On the basis of its critical roles in physiology and pathology, AMPK is emerging as one of the most promising targets for both the prevention and treatment of these diseases. In this review, we discuss the current understanding of the molecular and physiological regulation of AMPK and its metabolic and physiological functions. In addition, we discuss the mechanisms underlying the versatile roles of AMPK in diabetes and cancer.
AMP-Activated Protein Kinases* ; Chronic Disease ; Homeostasis ; Inflammation ; Obesity ; Pathology ; Phosphotransferases ; Physiological Processes ; Physiology* ; Protein Kinases